Indoor air quality is a term which refers to the air quality within and around buildings and structures, especially as it relates to the health and comfort of building occupants. Indoor air quality can be affected by gases, particulates, biological contaminants, bacteria or any mass or energy stressor that can induce adverse health conditions. Representatives among the gases are volatile organic chemicals (VOC) including benzene, formaldehyde, pentachlorobenzene, toluene, xylene and styrene, and radon. Biological contaminants of indoor air may include bacteria, mould, viruses, house dust mites, cockroaches, cat dandruff, saliva, and pollen. Particularly, floating micron or sub-micron sized secretions from house dust mites, mould, pet, cockroaches, and bacteria, when inhaled, induce an immune response, resulting in the onset of inflammatory respiratory diseases.
Various kinds of bacteria and mould are found in indoor air and these inhabit the skin, the gastrointestinal tract and respiratory tract of many different organisms such as humans, pets, house dust mites and cockroaches and live or are introduced from inside or around buildings and structures.
Examples of the bacteria that are found in indoor air include Bacillus sp., Staphylococcus aureus, Staphylococcus epidermidis, Staphylococcus hominis, Pseudomonas stutzeri, Pseudomonas luteola, Streptomycetes, Corynebacteriaceae, and Escherichia coli. 
These various bacterial air pollutants and their endotoxins (lipopolysaccharide, LPS) or peptidoglycans are known to induce the production of inflammatory cytokines from immune cells and lung epithelial cells.
Meanwhile, Gram-negative bacteria constitutively secrete outer membrane vesicles into the extracellular milieu. Extracellular vesicles secreted from Gram-negative bacteria are spherical with a size of 20-200 nm and consist of phospholipid bilayers. Gram-negative bacterial extracellular vesicles have LPS as well as various outer membrane proteins that can regulate inflammatory responses in host cells. Recently, the present inventors have reported that Gram-positive bacteria also secrete extracellular vesicles and that the extracellular vesicles contain proteins capable of inducing inflammation as analyzed by proteomic analysis.
Inflammatory respiratory diseases may be largely classified by the organ or tissue involved, for example, as upper respiratory tract infections, such as rhinitis and sinusitis, lower respiratory tract infections, such as asthma and bronchitis, small air way diseases such as bronchiolitis, and lung parenchymal diseases such as emphysema and pneumonia. From the view of clinical obstruction of the airway, respiratory diseases may be classified as asthma characterized by reversible obstruction and chronic obstructive pulmonary disease (COPD) characterized by irreversible obstruction. Chronic obstructive pulmonary disease is the co-occurrence of chronic obstructive bronchitis or chronic obstructive bronchiolitis and emphysema. A lot about allergic asthma is associated with sensitivity to indoor proteins (allergens), and so a lot of attention has focused on the increased exposure to these allergens as being the primary cause of the rise in asthma cases. Irritants such as those from smoking are associated with a greater risk of chronic obstructive pulmonary disease.
The importance of inflammation in the onset of asthma and chronic obstructive pulmonary disease have been previously reported, but inflammation patterns differ therebetween. Eosinophilic inflammation is a pathogenic correlate of asthma while non-eosinophilic or neutrophilic inflammation is responsible for chronic obstructive pulmonary disease. Rather, neutrophils accumulate in the airways in patients with asthma who have more severe airflow obstruction, where an excess of eosinophils may also be present. In addition, neutrophils are prominent in airway secretions during acute asthma, especially irreversible asthma exacerbations. Further, the etiology of chronic inflammation in the lung may be accounted for by the immune dysfunction generated in the trachea and the lung paranchyma. The present inventors previously reported that eosinophilic inflammation is associated with Th2 immune responses while neutrophilic inflammation is associated with Th1 and Th17 immune responses. It has long been suggested that inflammation may develop into cancer. Recent reports showed that Th17-mediated immune responses to a toxin derived from gut flora are associated with the onset of colorectal cancer. Helicobacter pylori, playing an important role in the natural stomach ecology, is known to cause not only chronic gastritis but also stomach cancer. It has been postulated that the same factor may be responsible for the etiology of both chronic obstructive pulmonary disease and lung cancer, which is supported by recent clinical studies that have showed that chronic obstructive pulmonary disease itself is an important risk factor for lung cancer, irrespective of smoking.